Brain Research最新文献

{"title":"Expression of concern: \"Protective effects of propofol against whole cerebral ischemia/reperfusion injury in rats through the inhibition of the apoptosis-inducing factor pathway\" [Brain Res. 1644 (2016) 9-14].","authors":"Tao Tao, Chun-Lei Li, Wan-Chao Yang, Xian-Zhang Zeng, Chun-Yu Song, Zi-Yong Yue, Hong Dong, Hua Qian","doi":"10.1016/j.brainres.2026.150345","DOIUrl":"10.1016/j.brainres.2026.150345","url":null,"abstract":"","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1885 ","pages":"150345"},"PeriodicalIF":2.6,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147863585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of concern: \"Propofol improved neurobehavioral outcome of cerebral ischemia-reperfusion rats by regulating Bcl-2 and Bax expression\" [Brain Res. 1410 (2011) 24-32].","authors":"Hong-Jie Xi, Tian-Hua Zhang, Tao Tao, Chun-Yu Song, Shu-Jun Lu, Cui, Zi-Yong Yue","doi":"10.1016/j.brainres.2026.150342","DOIUrl":"10.1016/j.brainres.2026.150342","url":null,"abstract":"","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1885 ","pages":"150342"},"PeriodicalIF":2.6,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147863536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Increased hemispheric functional connectivity compensates speech perception in older adults with hearing loss","authors":"Yi Liu ,&nbsp;Junhua Ding ,&nbsp;Songjian Wang ,&nbsp;Nuonan Kou ,&nbsp;Shuo Wang","doi":"10.1016/j.brainres.2026.150201","DOIUrl":"10.1016/j.brainres.2026.150201","url":null,"abstract":"<div><div>Age-related hearing loss (ARHL) is associated with widespread cortical reorganization, yet the adaptive mechanisms of functional connectivity across disease stages and brain states remain unclear. Using functional near-infrared spectroscopy (fNIRS), we examined both resting-state and speech perception-evoked functional connectivity (FC) in older adults with normal hearing, mild hearing loss, or moderate-to-severe hearing loss. FC alterations were found to be both state-dependent (i.e., varying with the cognitive state) and stage-dependent (i.e., depending on the severity of hearing loss). At rest, only the most impaired group showed localized increases in right-hemispheric FC. During speech perception, the mildly impaired group exhibited widespread FC enhancements across cross-hemispheric networks. These task-evoked enhancements were absent in the severely impaired group, suggesting a breakdown in adaptive recruitment. Subnetwork-level analyses further revealed spatially specific alterations in right-lateralized frontoparietal and frontotemporal circuits, as well as interhemispheric pathways linking left-hemisphere language hubs with right-hemisphere regions supporting attention, executive function, and top-down linguistic prediction. Collectively, our findings delineate a nonlinear trajectory of neural adaptation in ARHL, highlight a temporally bounded window of plasticity in early stages, and underscore the essential role of cross-hemispheric reorganization in sustaining speech processing under cognitive load.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1876 ","pages":"Article 150201"},"PeriodicalIF":2.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146149000","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of repopulated microglia-associated genes in microglia depleted/repopulated mice after spinal cord injury","authors":"Shiyuan Xue ,&nbsp;Die Hu ,&nbsp;Liping Li ,&nbsp;Yuerong Sun ,&nbsp;Xinyi Wei ,&nbsp;Yan Xiao ,&nbsp;Qiling Jiang ,&nbsp;Chao Qi ,&nbsp;Haitao Fu","doi":"10.1016/j.brainres.2026.150189","DOIUrl":"10.1016/j.brainres.2026.150189","url":null,"abstract":"<div><div>This study aimed to investigate the effects of repopulated microglia on neural repair and functional recovery and identify repopulated microglia-associated repair-promoting genes after spinal cord injury (SCI) in mice following depletion of microglia via the colony-stimulating factor 1 receptor (CSF1R) inhibitor PLX3397. Mice were divided into control, sustained microglial depletion, and microglial depletion/repopulation groups according to being treated standard or PLX3397 diet. Mice in all groups were subjected to a complete spinal cord crush injury. Comprehensive assessments were performed using behavioral scoring, immunofluorescence staining 21 days post-injury, and RNA sequencing 21 days post-injury. Results demonstrated that PLX3397 effectively eliminated approximately 95 % of microglia in the mouse spinal cord. Upon drug withdrawal, microglia rapidly repopulated and exhibited a pro-regenerative phenotype. Repopulated microglia significantly promoted post-injury motor functional recovery, increased neuronal survival, and reduced glial scar formation. Transcriptomic analysis identified genes associated with repopulated microglia, which were enriched in immune response, complement activation, phagocytosis, and cytokine signaling pathways. Protein-protein interaction (PPI) network analysis of these associated genes further pinpointed key genes, including<!--> <em>Il1b</em>,<!--> <em>Ccr2</em>, and <em>Il15</em>. This study reveals that repopulated microglia may exert neuroprotective effects by modulating the immune microenvironment. The 336 repopulated microglia-associated genes identified in this study, and the identified key genes that are preferentially upregulated in repopulated microglia may represent novel therapeutic targets for SCI.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1876 ","pages":"Article 150189"},"PeriodicalIF":2.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146112387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ghrelin-based interventions in preclinical models of Parkinson’s disease: a systematic review","authors":"Henrique José Cavalcanti Bezerra Gouveia ,&nbsp;Osmar Henrique dos Santos-Júnior ,&nbsp;Johannes Frasnelli ,&nbsp;Alexandre Fisette ,&nbsp;Joaci Pereira dos Santos Júnior ,&nbsp;Marcos Antônio da Silva Araújo ,&nbsp;Eulália Rebeca da Silva-Araújo ,&nbsp;Ana Elisa Toscano ,&nbsp;Raul Manhães de Castro","doi":"10.1016/j.brainres.2026.150187","DOIUrl":"10.1016/j.brainres.2026.150187","url":null,"abstract":"<div><div>Ghrelin plays a crucial role in metabolism and gastrointestinal function. In the central nervous system, ghrelin modulates both hedonic and homeostatic control of eating behavior. Ghrelin promotes neuron survival by reducing apoptosis, inflammation, and oxidative stress, making it a potential therapeutic agent for neurodegenerative diseases. Parkinson’s Disease (PD) is a neurodegenerative disease characterized by motor and non-motor symptoms. The motor impairments result primarily from the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta. Individuals with PD exhibit reduced levels of fasting and postprandial plasma ghrelin, and its receptors (GHSR) are expressed in the substantia nigra. Thus, this review aimed to evaluate the effects of ghrelin or GHSR agonists administration in experimental models of PD. A systematic search was conducted across PubMed, Scopus, Web of Science, and Embase. The 12 included studies involved PD models induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), 6-hydroxydopamine (6-OHDA), as well as A53T transgenic mice. Interventions were performed with acylated and/or des-acylated ghrelin, in addition to the GHSR agonist HM01. Intervention with ghrelin was able to reduce dopaminergic neurodegeneration and improve motor function, while also positively impacting metabolic and gastrointestinal functions, expanding its relevance to non-motor consequences of PD. Considering that most results were obtained using acute toxin-induced models and only male animals, further studies using progressive PD models and evaluating sex differences are needed. Thus, although preclinical evidence supports ghrelin or GHSR agonists as promising agents for treatment, future studies will be essential to inform clinical translation and optimize therapeutic strategies for individuals with PD.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1876 ","pages":"Article 150187"},"PeriodicalIF":2.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146123847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alpha suppression during non-painful tactile stimulation","authors":"Çağdaş Güdücü ,&nbsp;Güliz Akın Öztürk ,&nbsp;Zehra Ülgen","doi":"10.1016/j.brainres.2026.150191","DOIUrl":"10.1016/j.brainres.2026.150191","url":null,"abstract":"<div><div>Alpha-band power is considered as a marker of sensory processing–related cortical states, including sensory suppression and the temporal organization of sensory input. This study aimed to investigate whether alpha-band power of electrophysiological brain responses is modulated by different interstimulus intervals during repetitive, non-painful tactile stimulation. Non-painful tactile stimuli were delivered to the index finger of the right hand with different interstimulus intervals (ISI) of 2 s (s), 4 s, and 8 s via a pneumatic stimulator. A separate session was conducted for each ISI in a pseudorandomized order. The electroencephalogram was recorded in all sessions with 24 volunteers. The results of the analysis showed that the alpha activity was lowest at ISI₄ and highest at ISI₈. This pattern was consistently observed in both the central and parietal regions. In the ISI₂ session, although no notable variation among the frontal, central, and parietal areas was observed, the most pronounced activity was observed in the frontal region in the ISI₄ session. The highest level of alpha activity was observed in the central area during the ISI₈ session. Variations in interstimulus intervals affect inhibitory control and sensory processing in the brain. The frontal cortex appears to manage attention and cognitive control more efficiently at intermediate intervals (ISI₄), whereas the central region shows greater involvement in processing tactile inputs at longer intervals (ISI₈).</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1876 ","pages":"Article 150191"},"PeriodicalIF":2.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146137031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of the dentate gyrus of hippocampus on acute pain modulation: Investigating of dopaminergic-opioidergic interactions in pain-related behaviors in the tail-flick test","authors":"Sahar Sadeghzadeh Sotoudeh ,&nbsp;Shima Abtin ,&nbsp;Roghayeh Mozafari ,&nbsp;Abbas Haghparast","doi":"10.1016/j.brainres.2026.150155","DOIUrl":"10.1016/j.brainres.2026.150155","url":null,"abstract":"<div><div>Previous studies have shown that injections of opioid and dopamine agonists alone into the dentate gyrus (DG) increase the threshold for acute pain responses. Therefore, this study aimed to investigate whether the opioid and D1-like dopamine receptor (D1R) interact to modulate acute pain in DG. One hundred and forty-seven adult male Wistar rats were cannulated unilaterally in the DG. Separate groups of animals received different doses of SCH23390 (6, 12, and 24 mmol/0.5 μL), a D1R antagonist, before injection of an effective dose of morphine (25 mmol/0.5 μL). In another experiment, animals received different naloxone (5, 15, and 45 mmol/0.5 μL) dose, an opioid receptor antagonist, before administering the effective dose of SKF38393 (6 mmol/0.5 μL). Acute pain threshold was assessed using the tail-flick test. Behavioral data analysis indicated that blockade of D1R in the DG significantly attenuated morphine-induced antinociception (P &lt; 0.001). Furthermore, the antinociceptive effects of SKF38393 were significantly reduced by blocking opioid receptors in the DG (P &lt; 0.01). Interestingly, the effect of SCH23390 in reducing the antinociceptive effects of morphine (η2 = 0.65) was numerically higher than the effect of naloxone in reducing the antinociceptive effects of SKF38393 (η2 = 0.46). The results suggest a strong interaction between opioidergic and dopaminergic systems in the DG in modulating acute pain. These findings can be used to reveal the precise mechanisms of pain modulation in brain circuits and to develop new strategies in pain management with greater efficacy and fewer side effects.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1875 ","pages":"Article 150155"},"PeriodicalIF":2.6,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145942368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of neurobiochemical and behavioral responses to carvone nanoemulsion: A neuroprotective approach for Alzheimer’s disease-associated dementia in a rat model","authors":"Sahand Kabiri ,&nbsp;Pariya Gholizadeh Dangheralou ,&nbsp;Farnaz Khazaeifard ,&nbsp;Samir Rostami Mehr ,&nbsp;Seyedeh Mohadeseh Mansouri ,&nbsp;Nahal Rahimi Rad ,&nbsp;Saeid Abbasi-Maleki","doi":"10.1016/j.brainres.2026.150143","DOIUrl":"10.1016/j.brainres.2026.150143","url":null,"abstract":"<div><h3>Background</h3><div>Antioxidant supplements have emerged as promising strategies to mitigate the impact of Alzheimer’s disease (AD) and associated dementia. We explored the neuroprotective potential of Carvone nanoemulsion (CANO) using a rat model of AD-associated dementia.</div></div><div><h3>Method</h3><div>Our experimental groups comprised non-AD control rats (CON), untreated AD rats (AD), and AD rats treated with CANO at two different dosages: 40 mg/kg (CANO40) and 80 mg/kg (CANO80). We assessed various behavioral parameters, malondialdehyde (MDA) and brain-derived neurotrophic factor (BDNF) levels,<!--> <!-->ferric-reducing ability of plasma (FRAP).</div></div><div><h3>Results</h3><div>AD induction caused a significant reduction in step-through latency (P &lt; 0.001), center time (P &lt; 0.001), the number of visits (P &lt; 0.001), and total distance traveled (P &lt; 0.001), time spent in open arms (P &lt; 0.001), and both FRAP (P &lt; 0.001) and BDNF levels (P &lt; 0.001) in comparison to the CON group, while elevating escape latency, time in target zone and platform location latency, and MDA levels (P &lt; 0.001). Treatment with CANO, particularly at the CANO80 dosage, significantly improved these parameters compared to the AD group, resulting in decreased time in the target zone (P &lt; 0.001), escape latency (P &lt; 0.001), and platform location latency (P &lt; 0.001) and higher FRAP (P &lt; 0.05) and BDNF levels (P &lt; 0.05), along with decreased MDA levels (P &lt; 0.05).</div></div><div><h3>Conclusion</h3><div>CANO, especially at the 80 mg/kg dosage, shows promise in alleviating symptoms associated with AD-associated dementia. However, further research is warranted to validate and expand upon these findings.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1875 ","pages":"Article 150143"},"PeriodicalIF":2.6,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145899448","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Covert attention modulates visual perception in early infancy","authors":"Shuma Tsurumi ,&nbsp;So Kanazawa ,&nbsp;Masami K. Yamaguchi ,&nbsp;Jun-ichiro Kawahara","doi":"10.1016/j.brainres.2026.150186","DOIUrl":"10.1016/j.brainres.2026.150186","url":null,"abstract":"<div><div>Visual attention enhances perception by facilitating detection, localization, and identification of stimuli. Classic accounts propose that such modulation depends on feedback from higher cortical areas, whereas recent evidence suggests contributions from feedforward processes within early visual regions. Infants provide a unique opportunity to test these mechanisms because their feedback pathways remain immature during the first half of the first year. Here, we examined whether covert attention influences perception in 3- to 4-month-old infants using a spatial cueing task. In Experiment 1, infants discriminated orientation, and in Experiment 2, they discriminated motion direction of cued peripheral gratings, despite not making eye movements. These findings demonstrate that covert attention modulates perception in early infancy, indicating that attentional effects can emerge via feedforward processes before the maturation of top–down feedback.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1875 ","pages":"Article 150186"},"PeriodicalIF":2.6,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146075108","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Programmed cell death pathways in Parkinson’s disease: Spotlight on ferroptosis and pyroptosis","authors":"Veerta Sharma,&nbsp;Reet Verma,&nbsp;Prateek Sharma,&nbsp;Thakur Gurjeet Singh","doi":"10.1016/j.brainres.2026.150165","DOIUrl":"10.1016/j.brainres.2026.150165","url":null,"abstract":"<div><div>Parkinson’s disease (PD) characterized by the selective loss of dopaminergic neurons in the brain resulting in motor and cognitive deficits. While apoptosis has long been considered a primary mechanism of neuronal death in PD, emerging evidence highlights the significant roles of non-apoptotic programmed cell death pathways, particularly ferroptosis and pyroptosis-in driving PD progression. Ferroptosis is form of cell death that is dependent on iron and driven by lipid peroxidation, appears to be associated with PD. On the other hand, Pyroptosis, a caspase-1-dependent inflammatory cell death pathway mediated by activation of inflammasome and release of pro-inflammatory cytokines such as interleukin-1β (IL-1β) and IL-18. Both pathways contribute to the neurodegeneration in PD through distinct yet interconnected pathways. Therefore, this review highlights molecular mechanisms underlying ferroptosis and pyroptosis in PD and recent advances in pharmacological strategies targeting these pathways.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1875 ","pages":"Article 150165"},"PeriodicalIF":2.6,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145965149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}